Cellular signalling最新文献

{"title":"LLGL2 targets the Hedgehog signaling pathway to influence malignant progression of endometrial cancer","authors":"Hua Yang ,&nbsp;Yuqing Ji ,&nbsp;Dong Liu ,&nbsp;Ou Chai ,&nbsp;Zhiying Qi ,&nbsp;Ruimeng Guo ,&nbsp;Bei Sun ,&nbsp;Fang Wang","doi":"10.1016/j.cellsig.2024.111553","DOIUrl":"10.1016/j.cellsig.2024.111553","url":null,"abstract":"<div><h3>Background</h3><div>Endometrial cancer (EC) is a malignant tumor of the endometrial epithelium, with endometrial adenocarcinoma being the most common type. It has a good overall prognosis, but recurrence and metastasis are often associated with poorer outcomes. LLGL2 is closely linked to tumorigenesis; however, its in endometrial carcinoma is unknown. This study investigated the biological function of LLGL2 in endometrial cancer and its intrinsic molecular mechanisms in promoting the malignant progression of the disease.</div></div><div><h3>Methods</h3><div>The expression of LLGL2 in endometrial cancer was analyzed using the TCGA database via UALCAN and validated through western blot analysis, RT-qPCR, and immunohistochemistry. Additionally, the correlation between LLGL2 and the clinicopathological features of patients was examined. The effects of LLGL2 on the proliferation and migration of endometrial cancer cells were assessed using EdU proliferation assay, clone formation assay, Transwell assay, scratch assay, and the detection of proliferation and metastasis markers. Furthermore, the impact of LLGL2 on key genes of the Hedgehog signaling pathway, including SHH, PTCH1, SMO, and GLI1, was explored using western blot analysis and RT-qPCR. The expression of SHH, PTCH1 and GLI1 was also detected in cells treated with the Hedgehog signaling pathway inhibitor (JK184) in endometrial cancer cells overexpressing LLGL2. Finally, the role of LLGL2 in tumor growth was investigated in vivo using sh-LLGL2 and OE-LLGL2 nude mouse tumorigenic model.</div></div><div><h3>Results</h3><div>LLGL2 expression was upregulated in endometrial cancer tissues compared to normal endometrium. LLGL2 expression was significantly correlated with tumor histological grading (<em>p</em> &lt; 0.01). LLGL2 promoted proliferation, migration, and invasive abilities of endometrial cancer cells. In the nude mouse tumorigenic model, LLGL2 deficiency inhibited the growth of subcutaneously transplanted tumors, and overexpression of LLGL2 promoted the growth of tumors. At the molecular level, LLGL2 may promote the transduction of the Hedgehog signaling pathway in endometrial cancer cells.</div></div><div><h3>Conclusion</h3><div>LLGL2 may be involved in the development of endometrial cancer as an oncogene, leading to aberrant activation of the Hedgehog signaling pathway. Therefore, LLGL2 is a potential new target for the treatment of endometrial cancer.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"127 ","pages":"Article 111553"},"PeriodicalIF":4.4,"publicationDate":"2024-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142794533","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SSBP1 positively regulates RRM2, affecting epithelial mesenchymal transition and cell cycle arrest in human lung adenocarcinoma cells","authors":"Xingyu Yang ,&nbsp;Bingfeng Ma ,&nbsp;Yafeng Liu ,&nbsp;Jiawei Zhou ,&nbsp;Jianqiang Guo ,&nbsp;Yuanyuan Peng ,&nbsp;Ying Bai ,&nbsp;Jing Wu ,&nbsp;Dong Hu","doi":"10.1016/j.cellsig.2024.111552","DOIUrl":"10.1016/j.cellsig.2024.111552","url":null,"abstract":"<div><div>Progression of lung adenocarcinoma (LUAD) is frequently associated with alterations in epithelial-mesenchymal transition (EMT) and cell cycle. Our study analyzed the Cancer Genome Atlas (TCGA) database and identified a positive correlation between high expression of SSBP1 in LUAD tumor tissues and poor prognosis (<em>p</em> &lt; 0.05), with an AUC of 0.853, suggesting that SSBP1 could serve as a prognostic biomarker. In vitro experiments, including siRNA-mediated SSBP1 knockdown and subsequent cell cloning and Transwell assays, revealed significant inhibition of proliferation, migration, and cell cycle progression in LUAD cells (<em>p</em> &lt; 0.05). In vivo mouse model experiments further confirmed that SSBP1 knockdown inhibits tumor burden (p &lt; 0.05). Mechanistic investigations, integrating pathway enrichment analysis with molecular biology techniques, identified RRM2 as a downstream target of SSBP1, and RRM2 knockdown similarly suppressed LUAD cell proliferation, migration, and cell cycle progression (<em>p</em> &lt; 0.05). These findings indicate that SSBP1 promotes EMT and cell cycle progression in LUAD cells by positively regulating RRM2, thereby accelerating disease progression. Collectively, our study not only confirms the potential role of SSBP1 in LUAD but also provides a theoretical foundation for therapeutic strategies targeting the SSBP1/RRM2 axis, potentially offering new therapeutic targets for LUAD patients.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"127 ","pages":"Article 111552"},"PeriodicalIF":4.4,"publicationDate":"2024-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142791214","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PTPN22 and the pathogenesis of ulcerative colitis: Insights into T cell differentiation and the JAK/STAT signaling pathway","authors":"Yang Yu ,&nbsp;Xinlei Ba ,&nbsp;Tong Li ,&nbsp;Wenying Xu ,&nbsp;Jiahui Zhao ,&nbsp;Na Zhang ,&nbsp;Yanjiao Zhao ,&nbsp;Tao Wang ,&nbsp;Xiaonan Zhang ,&nbsp;Xipeng Wang ,&nbsp;Bin Bai ,&nbsp;Bing Wang","doi":"10.1016/j.cellsig.2024.111551","DOIUrl":"10.1016/j.cellsig.2024.111551","url":null,"abstract":"<div><div>70 % of the ulcerative colitis (UC) linked gene loci are associated with other autoimmune or immunodeficient diseases. The phosphatase activity of PTPN22 can regulate the development of T cells and contribute to regulate the level of inflammation in autoimmune diseases. We produced PTPN22-CS thymus-specific transgenic mice, which suppressed PTPN22 enzyme activity in the thymocytes. Overexpressed PTPN22-CS facilitated the development of the thymocytes towards CD4⁺T cells and resulted in an increased proportion of the Th1 and Treg cells in the UC mesenteric lymph nodes. PTPN22-CS promoted the activation of the JAK/STAT signaling pathway in the Th1 and Treg cells that localized in the colon, resulting in an excessive production of inflammatory mediators such as IL-2 and IFN-γ. Consequently, PTPN22-CS contributes to the inflammatory response of ulcerative colitis. In summary, the tyrosine phosphatase activity of PTPN22 plays a role in modulating UC by regulating T cell differentiation and modulating the JAK/STAT signaling pathway, thereby influencing the inflammatory response in colonic. These findings provide new insight into the association between PTPN22 and the pathogenesis of UC.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"127 ","pages":"Article 111551"},"PeriodicalIF":4.4,"publicationDate":"2024-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142791212","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “Fangchinoline inhibits metastasis and reduces inflammation-induced epithelial-mesenchymal transition by targeting the FOXM1-ADAM17 axis in hepatocellular carcinoma” [Cell Signal. 2024 Dec:124:111467]","authors":"Liyun Zheng ,&nbsp;Vinothkumar Rajamanickam ,&nbsp;Mengyuan Wang ,&nbsp;Huajun Zhang ,&nbsp;Shiji Fang ,&nbsp;Michael Linnebacher ,&nbsp;A.M. Abd El-Aty ,&nbsp;Xinbin Zhang ,&nbsp;Yeyu Zhang ,&nbsp;Jianbo Wang ,&nbsp;Minjiang Chen ,&nbsp;Zhongwei Zhao ,&nbsp;Jiansong Ji","doi":"10.1016/j.cellsig.2024.111542","DOIUrl":"10.1016/j.cellsig.2024.111542","url":null,"abstract":"","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"127 ","pages":"Article 111542"},"PeriodicalIF":4.4,"publicationDate":"2024-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142784227","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibition of XIST restrains paclitaxel resistance in breast cancer cells by targeting hsa-let-7d-5p/ATG16L1 through regulation of autophagy","authors":"Yueyue Wang ,&nbsp;Wenhao Pei ,&nbsp;Yuping Yang ,&nbsp;Chaoqun Xia ,&nbsp;Qiang Zhang ,&nbsp;Zhijun Geng ,&nbsp;Xiuru Shi ,&nbsp;Fengchao Wang","doi":"10.1016/j.cellsig.2024.111534","DOIUrl":"10.1016/j.cellsig.2024.111534","url":null,"abstract":"<div><div>Breast cancer is a fatal malignant tumor in women worldwide. The development of paclitaxel resistance remains a challenge. Autophagy is considered to have a significant part in the chemotherapeutic stress mechanism. This study aimed to investigate the function of long non-coding RNA (lncRNA) in breast cancer cell chemoresistance and autophagy. The paclitaxel (PTX)-resistant breast cancer cells were established. The function of X-inactive specific transcript (XIST) was demonstrated using in vitro and in vivo experiments. Transmission electron microscope (TEM) was used to observe autophagy vesicles. Protein and mRNA levels were determined using western blotting and quantitative real time polymerase chain reaction (qRT-PCR). We discovered that autophagic activity was correlated with chemoresistance in PTX-resistant breast cancer cells. In vitro and in vivo studies showed that XIST inhibition reduced cell resistance to paclitaxel, caused autophagy to be suppressed by regulating hsa-let-7d-5p and ATG16L1 expression. Mechanically, threonine protein kinase B (PKB; also known as AKT) - mammalian target of rapamycin (mTOR) pathway was activated when knockdown of XIST, while was reversed by inhibition of hsa-let-7d-5p. Our results verified that XIST played a significant role in developing chemoresistance via mediating autophagy in PTX-resistant breast cancer cells. It may be a potential target for breast cancer treatment strategies.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"127 ","pages":"Article 111534"},"PeriodicalIF":4.4,"publicationDate":"2024-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142784228","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"AIM2 promotes the progression of HNSCC via STAT1 mediated transcription and IL-17/MAPK signaling","authors":"Dong Ding ,&nbsp;Hongfei Liu ,&nbsp;Liping Zhang ,&nbsp;Guoxin Zhang ,&nbsp;Yumin Wei ,&nbsp;Wenlong Zhang ,&nbsp;Xingjiu Yang ,&nbsp;Mengyuan Li ,&nbsp;Gaofei Yin ,&nbsp;Wei Guo ,&nbsp;Xiaohong Chen ,&nbsp;Zhigang Huang ,&nbsp;Ran Gao","doi":"10.1016/j.cellsig.2024.111545","DOIUrl":"10.1016/j.cellsig.2024.111545","url":null,"abstract":"<div><div>Chronic inflammation has been recognized as one of the hallmarks of head and neck squamous cell carcinoma (HNSCC), Absent In Melanoma 2(AIM2) has emerged as important regulators of chronic inflammatory, and participated in initiation, progression of kinds of human cancers. Nonetheless, the biological functions and underlying mechanisms of AIM2 in HNSCC remain inadequately understood. Based on the bioinformatics analysis of public databases, we identified elevated AIM2 expression in HNSCC, which positively correlates with disease stage and HPV infection, thereby possessing both diagnostic and prognostic significance. Immunohistochemistry on clinical samples revealed that AIM2 expression was frequently upregulated in cancerous tissues compared to paracancerous tissues, exhibiting a significant association with Ki-67 expression. Modulating AIM2 expression in HNSCC cell lines through transfection with inhibitors or mimics demonstrated that ectopic AIM2 expression enhances cell growth, migration, tumorigenesis, and metastasis both in vitro and in vivo. A dual luciferase reporter assay indicated that the transcription factor STAT1 can bind directly to the AIM2 promoter region and activate its transcription. The STAT1 inhibitor, fludarabine, reduces AIM2 expression and subsequently diminishes cell proliferation. Mechanistically, AIM2 exerts its tumor-promoting effects through the IL-17-MAPK signaling pathway. Collectively, our data demonstrate that AIM2, transcriptionally activated by STAT1, exhibits oncogenic functions by promoting the IL-17-MAPK signaling pathway, suggesting that AIM2 may be a new intervention targets for the diagnostic and treatment of HNSCC.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"127 ","pages":"Article 111545"},"PeriodicalIF":4.4,"publicationDate":"2024-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142784226","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypoxia regulates small extracellular vesicle biogenesis and cargo sorting through HIF-1α/HRS signaling pathway in head and neck squamous cell carcinoma","authors":"Yiman Wang ,&nbsp;Bolin Xiao ,&nbsp;Jinbang Li ,&nbsp;Mengyao Zhang ,&nbsp;Linzhou Zhang ,&nbsp;Liguo Chen ,&nbsp;Jing Zhang ,&nbsp;Gang Chen ,&nbsp;Wei Zhang","doi":"10.1016/j.cellsig.2024.111546","DOIUrl":"10.1016/j.cellsig.2024.111546","url":null,"abstract":"<div><div>Small extracellular vesicles (sEVs) act as crucial messengers that transmit biological signals in hypoxic tumor microenvironment (TME), significantly impacting cancer progression. However, the precise mechanism by which hypoxia influences sEV biogenesis remains poorly understood. In this study, we observed increased sEV secretion and alterations in cargo composition in head and neck squamous cell carcinoma (HNSCC) cells under hypoxic conditions. We found that hepatocyte growth factor–regulated tyrosine kinase substrate (HRS), a key component of the endosomal sorting complexes required for transport (ESCRT), was upregulated during hypoxia. This upregulation activated the endosomal system and reduced degradation of multivesicular bodies (MVBs). HRS depletion altered the packaging of protein cargoes such as mitochondria-related proteins into sEVs under hypoxia, and these cargoes promoted a pro-tumorigenic phenotype of macrophages. Importantly, we demonstrated that HRS is transcriptionally activated by hypoxia inducible factor-1α (HIF-1α). Spatial transcriptomics and immunohistochemistry revealed a positive correlation between HRS and HIF-1α. These findings establish a link between the hypoxic response, sEV biogenesis, and cargo packaging, enhancing our understanding of how the hypoxic TME influences sEV biogenesis in HNSCC cells.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"127 ","pages":"Article 111546"},"PeriodicalIF":4.4,"publicationDate":"2024-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142779613","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microtubule-Rab5 mutual-influential system screening based on gene-regulatory networks map in Rab5 RNAi eye-degeneration model","authors":"Yuyu Nan ,&nbsp;Jingjing Lin ,&nbsp;Zaiwa Wei ,&nbsp;Yufeng Yang ,&nbsp;Qinghua Li","doi":"10.1016/j.cellsig.2024.111544","DOIUrl":"10.1016/j.cellsig.2024.111544","url":null,"abstract":"<div><div>Rabs are involved in neuronal development and protrusion formation. Existing studies support the notion that manipulation or mutation of <em>Rab</em> genes could lead to functional changes in neurons. However, whether <em>Rabs</em> gene-manipulation induced <em>Drosophila</em> eye-degeneration remains unknown. By down-regulating <em>Rab5</em>, but not <em>Rab7</em>, we first constructed a compound eye injury model in <em>Drosophila</em>. As the distribution, content, and even maturation of Rab5-positive endosomes are influenced by cytoskeletal proteins, like actin or tubulin-related proteins, the existence of a bidirectional regulatory relationship between Rab5 and the cytoskeleton remains unclear and worth researching. Through complete transcriptome sequencing combined immunofluorescence testing, we confirmed that down-regulation of <em>Rab5</em> affected the increase of α-Tub84B (alternatively named TubA84B) but not γ-tubulin. Based on Weighted Gene Co-Expression Network Analysis (WGCNA) and multi-tissue screening verification, this study proposes that the apoptosis-related factors–Rab5–TubA84B have conserved regulatory functions with cooperative expression. Gene manipulation confirmed that apoptotic factors, especially rpr, strongly regulate Rab5, and may ultimately influence microtubule structure through complex routes, including the Rab5 variance and the intracellular configuration ratio of α-Tubulin to Glyceraldehyde-3-phosphate dehydrogenase.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"127 ","pages":"Article 111544"},"PeriodicalIF":4.4,"publicationDate":"2024-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142779632","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"METTL3-mediated SMPDL3A promotes cell growth, metastasis and immune process of hepatocellular carcinoma by regulating LRPPRC","authors":"Weixin Xu ,&nbsp;Miaomiao Tao ,&nbsp;Yeqiong Liu ,&nbsp;Jun Yan ,&nbsp;Jiali Hu ,&nbsp;Lei Wang","doi":"10.1016/j.cellsig.2024.111543","DOIUrl":"10.1016/j.cellsig.2024.111543","url":null,"abstract":"<div><h3>Background</h3><div>Methyltransferase-like protein 3 (METTL3) has been confirmed to act as a tumor promoter to regulate hepatocellular carcinoma (HCC) progression. Therefore, more roles and mechanisms of METTL3 in HCC progression deserve to be further revealed.</div></div><div><h3>Methods</h3><div>The mRNA and protein levels of METTL3, sphingomyelin phodiesterase acid-like 3 A (SMPDL3A), and leucine rich pentatricopeptide repeat containing (LRPPRC) were determined by qRT-PCR and western blot. Cell proliferation, apoptosis, invasion and migration were detected by CCK8 assay, EdU assay, flow cytometry, transwell assay and wound healing assay. HCC cells were co-cultured with phytohemagglutinin-stimulated peripheral blood mononuclear cells, cytokine-induced killer cells, or CD8 + T-cells. IFN-γ, TNF-α levels, HCC cell survival rate and CD8 + T-cell apoptosis were determined to assess cell immune process. The interaction between METTL3, SMPDL3A and LRPPRC was assessed by MeRIP assay, RIP assay, dual-luciferase reporter assay or Co-IP assay. Animal experiments were performed to evaluate the effect of METTL3 knockdown on HCC tumorigenesis and lung metastasis.</div></div><div><h3>Results</h3><div>METTL3 was upregulated in HCC tissues and cells, and its knockdown repressed HCC cell proliferation, invasion, migration, immune process and promoted apoptosis. METTL3 increased SMPDL3A mRNA stability by m6A methylation modification, and this modification could be recognized by IGF2BP1. SMPDL3A overexpression reversed the inhibitory effect of METTL3 knockdown on HCC cell growth, metastasis and immune process. SMPDL3A interacted with LRPPRC to positively regulate its expression, and LRPPRC overexpression also eliminated the regulation of SMPDL3A silencing on HCC progression. In addition, downregulation of METTL3 repressed HCC tumorigenesis and lung metastasis <em>via</em> mediating SMPDL3A/LRPPRC axis.</div></div><div><h3>Conclusion</h3><div>METTL3 accelerated HCC cell growth, metastasis and immune process by regulating SMPDL3A/LRPPRC axis, providing a potential target for HCC treatment.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"127 ","pages":"Article 111543"},"PeriodicalIF":4.4,"publicationDate":"2024-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142779617","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expression of concern: The emerging crosstalk between atherosclerosis-related microRNAs and Bermuda triangle of foam cells: Cholesterol influx, trafficking, and efflux.","authors":"","doi":"10.1016/j.cellsig.2024.111394","DOIUrl":"10.1016/j.cellsig.2024.111394","url":null,"abstract":"","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"124 ","pages":"111394"},"PeriodicalIF":4.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142603112","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}